Migration-related influences on obesity among sub-Saharan African migrant adolescents in Melbourne, Australia

Aim: The aim of the present study was to examine migration- and socioeconomic-related influences on obesity among African migrant adolescents in Melbourne, Australia. Methods: Anthropometric data were collected from 99 parents and 100 adolescent offspring who also completed questionnaires eliciting demographic, socioeconomic and migration data. Multiple linear regressions were used to assess the relationship between migration- and socioeconomic-related factors and adolescent body mass index (BMI). Results: Only gender and parental BMI were associated with adolescent BMI after adjusting for adolescent age, adolescent gender, religion, parental BMI, parental education level and annual income. Boys (β=-1.45; P < 0.05) had lower BMI than girls. Parental and adolescent BMI were positively associated (β = 0.11; P < 0.05). In examining migration-related factors and adolescent BMI, after adjusting for gender and parental BMI, parental acculturation patterns and pre-migration life environment were associated with adolescent BMI, explaining, respectively, 6.5 and 4.0% of the variance in BMI. An integrated parental acculturation pattern was negatively associated with adolescent BMI (β=-0.17; P < 0.05) while adolescents whose parents came from rural areas had a higher BMI (β = 1.48; P < 0.05) than those whose parents came from urban areas. Adolescent acculturation patterns and length of stay in Australia were non-significantly associated with their BMI. Conclusions: Gender, pre-migration life environment and parental acculturation patterns seem to influence the prevalence of overweight and obesity among African migrant adolescents. Culturally competent obesity prevention programmes targeted towards African adolescents should consider these aspects in their design and delivery; however, further research is required to determine their relative contributions to African adolescent obesity in Australia.

Integrated phenotypic and activity-based profiling links Ces3 to obesity and diabetes

Phenotypic screening is making a comeback in drug discovery as the maturation of chemical proteomics methods has facilitated target identification for bioactive small molecules. A limitation of these approaches is that time-consuming genetic methods or other means are often required to determine the biologically relevant target (or targets) from among multiple protein-compound interactions that are typically detected. Here, we have combined phenotypic screening of a directed small-molecule library with competitive activity-based protein profiling to map and functionally characterize the targets of screening hits. Using this approach, we identify carboxylesterase 3 (Ces3, also known as Ces1d) as a primary molecular target of bioactive compounds that promote lipid storage in adipocytes. We further show that Ces3 activity is markedly elevated during adipocyte differentiation. Treatment of two mouse models of obesity-diabetes with a Ces3 inhibitor ameliorates multiple features of metabolic syndrome, illustrating the power of the described strategy to accelerate the identification and pharmacologic validation of new therapeutic targets.

Obesity prevention in early life: an opportunity to better support the role of Maternal and Child Health Nurses in Australia

BACKGROUND: Because parents with young children access primary health care services frequently, a key opportunity arises for Maternal and Child Health (MCH) nurses to actively work with families to support healthy infant feeding practices and lifestyle behaviours. However, little is known regarding the extent to which MCH nurses promote obesity prevention practices and how such practices could be better supported. METHODS: This mixed methods study involved a survey of 56 MCH nurses (response rate 84.8 %), 16 of whom participated in semi-structured qualitative interviews. Both components aimed to examine the extent to which nurses addressed healthy infant feeding practices, healthy eating, active play and limiting sedentary behavior during routine consultations with young children 0-5 years. Key factors influencing such practices and how they could be best supported were also investigated. All data were collected from September to December 2013. Survey data were analysed descriptively and triangulated with qualitative interview findings, the analysis of which was guided by grounded theory principles. RESULTS: Although nurses reported measuring height/length and weight in most consultations, almost one quarter (22.2 %) reported never/rarely using growth charts to identify infants or children at risk of overweight or obesity. This reflected a reluctance to raise the issue of weight with parents and a lack of confidence in how to address it. The majority of nurses reported providing advice on aspects of infant feeding relevant to obesity prevention at most consultations, with around a third (37 %) routinely provided advice on formula preparation. Less than half of nurses routinely promoted active play and only 30 % discussed limiting sedentary behaviour such as TV viewing. Concerns about parental receptiveness and maintaining rapport were key barriers to more effective implementation. CONCLUSION: While MCH nurses are well placed to address obesity prevention in early life, there is currently a missed public health opportunity. Improving nurse skills in behaviour change counseling will be key to increasing their confidence in raising sensitive lifestyle issues with parents to better integrate obesity prevention practices into normal MCH service delivery.

Migration, acculturation and environment: determinants of obesity among Iranian migrants in Australia

While migration from low- to high-income countries is typically associated with weight gain, the obesity risks of migration from middle-income countries are less certain. In addition to changes in behaviours and cultural orientation upon migration, analyses of changes in environments are needed to explain post-migration risks for obesity. The present study examines the interaction between obesity-related environmental factors and the pattern of migrant acculturation in a sample of 152 Iranian immigrants in Victoria, Australia. Weight measurements, demographics, physical activity levels and diet habits were also surveyed. The pattern of acculturation (relative integration, assimilation, separation or marginalization) was not related to body mass index, diet, or physical activity behaviours. Three relevant aspects of participants' perception of the Australian environment (physically active environments, social pressure to be fit, unhealthy food environments) varied considerably by demographic characteristics, but only one (physically active environments) was related to a pattern of acculturation (assimilation). Overall, this research highlighted a number of key relationships between acculturation and obesity-related environments and behaviours for our study sample. Theoretical models on migration, culture and obesity need to include environmental factors.

Welcome from the policies, socio-economic aspects, and health systems research section

At BMC Obesity, the Policies, Socio-economic Aspects, and Health Systems Research Section provides an opportunity to submit research focussed on what we need to know to support implementation of obesity policies most likely to achieve substantial, sustainable and equitable reductions in the prevalence of obesity globally. Here, we present the aims and objectives of this section, hearing from each of the Associate Editors in turn. The ambition of the Policies, Socio-economic Aspects, and Health Systems Research Section is to foster innovative research combining scientific quality with real world experience. We envisage this will include research addressing the structural drivers of obesity, solution oriented research, research addressing socio-economic inequalities in obesity and obesity prevention in low and middle income countries. We look forward to stimulating research to advance both the methods and substance required to drive uptake of effective and equitable obesity reduction policies globally.

Change of school in early adolescence and adverse obesity-related dietary behavior: a longitudinal cohort study, Victoria, Australia, 2013-2014

INTRODUCTION: Environments that facilitate energy-dense, nutrient-poor diets are associated with childhood obesity. We examined the effect of a change of school environment on the prevalence of obesity and related dietary behavior in early adolescence. METHODS: Fifteen schools in Victoria, Australia, were recruited at random from the bottom 2 strata of a 5-level socioeconomic scale. In 9 schools, students in grade 6 primary school transitioned to different schools for grade 7 secondary school, whereas in 6 schools, students remained in the same school from grade 6 to grade 7. Time 1 measures were collected from students (N = 245) in grade 6 (aged 11-13 y). Time 2 data were collected from 243 (99%) of the original cohort in grade 7. Data collected were dietary recall self-reported by students via questionnaire, measured height and weight of students, and aspects of the school food environment via school staff survey. Comparative and mixed model regression analyses were conducted. RESULTS: Of 243 students, 63% (n = 152) changed schools from time 1 to time 2, with no significant difference in weight status. Students who changed schools reported an increase in purchases of after-school snack food, greater sweetened beverage intake, fewer fruit-and-vegetable classroom breaks, and less encouragement for healthy eating compared with students who remained in the same school. School staff surveys showed that more primary than secondary schools had written healthy canteen policies and fewer days of canteen or food services operation. CONCLUSION: A change of school environment has negative effects on children's obesity-related dietary behavior. Consistent policy is needed across school types to support healthy eating in school environments.

A review of the relationship between socioeconomic position and the early-life predictors of obesity

A range of important early-life predictors of later obesity have been identified. Children of lower socioeconomic position (SEP) have a steeper weight gain trajectory from birth with a strong socioeconomic gradient in child and adult obesity prevalence. An assessment of the association between SEP and the early-life predictors of obesity has been lacking. The review involved a two-stage process: Part 1, using previously published systematic reviews, we developed a list of the potentially modifiable determinants of obesity observable in the pre-natal, peri-natal or post-natal (pre-school) periods; and part 2, conducting a literature review of evidence for socioeconomic patterning in the determinants identified in part 1. Strong evidence was found for an inverse relationship between SEP and (1) pre-natal risk factors (pre-pregnancy maternal body mass index (BMI), diabetes and pre-pregnancy diet), (2) antenatal/peri natal risk factors (smoking during pregnancy and low birth weight) and (3) early-life nutrition (including breastfeeding initiation and duration, early introduction of solids, maternal and infant diet quality, and some aspects of the home food environment), and television viewing in young children. Less strong evidence (because of a lack of studies for some factors) was found for paternal BMI, maternal weight gain during pregnancy, child sleep duration, high birth weight and lack of physical activity in young children. A strong socioeconomic gradient exists for the majority of the early-life predictors of obesity suggesting that the die is cast very early in life (even pre-conception). Lifestyle interventions targeting disadvantaged women at or before child-bearing age may therefore be particularly important in reducing inequality. Given the likely challenges of reaching this target population, it may be that during pregnancy and their child's early years are more feasible windows for engagement.

Effects of parent and child behaviours on overweight and obesity in infants and young children from disadvantaged backgrounds: systematic review with narrative synthesis

BACKGROUND: Despite the crucial need to develop targeted and effective approaches for obesity prevention in children most at risk, the pathways explaining socioeconomic disparity in children's obesity prevalence remain poorly understood.

METHODS: We conducted a systematic review of the literature that investigated causes of weight gain in children aged 0-5 years from socioeconomically disadvantaged or Indigenous backgrounds residing in OECD countries. Major electronic databases were searched from inception until December 2015. Key words identified studies addressing relationships between parenting, child eating, child physical activity or sedentary behaviour and child weight in disadvantaged samples.

RESULTS: A total of 32 articles met the inclusion criteria. The Mixed Methods Appraisal Tool quality rating for the studies ranged from 25 % (weak) to 100 % (strong). Studies predominantly reported on relationships between parenting and child weight (n = 21), or parenting and child eating (n = 12), with fewer (n = 8) investigating child eating and weight. Most evidence was from socio-economically disadvantaged ethnic minority groups in the USA. Clustering of diet, weight and feeding behaviours by socioeconomic indicators and ethnicity precluded identification of independent effects of each of these risk factors.

CONCLUSIONS: This review has highlighted significant gaps in our mechanistic understanding of the relative importance of different aspects of parent and child behaviours in disadvantaged population groups.

Prevention of childhood obesity

Childhood obesity is a complex disease with different genetic, metabolic, environmental and behavioural components that are interrelated and potentially confounding, thus making causal pathways difficult to define. Given the tracking of obesity and the associated risk factors, childhood is an important period for prevention. To date, evidence would support preventative interventions that encourage physical activity and a healthy diet, restrict sedentary activities and offer behavioural support. However, these interventions should involve not only the child but the whole family, school and community. If the current global obesity epidemic is to be halted, further large-scale, well-designed prevention studies are required, particularly within settings outside of the USA, in order to expand the currently limited evidence base upon which clinical recommendations and public health approaches can be formulated. This must be accompanied by enhanced monitoring of paediatric obesity prevalence and continued support from all stakeholders at global, national, regional and local levels.

Physical activity attenuates the effect of the FTO genotype on obesity traits in European adults: the Food4Me study

OBJECTIVE: To examine whether the effect of FTO loci on obesity-related traits could be modified by physical activity (PA) levels in European adults. METHODS: Of 1,607 Food4Me participants randomized, 1,280 were genotyped for FTO (rs9939609) and had available PA data. PA was measured objectively using accelerometers (TracmorD, Philips), whereas anthropometric measures [BMI and waist circumference (WC)] were self-reported via the Internet. RESULTS: FTO genotype was associated with a higher body weight [β: 1.09 kg per risk allele, (95% CI: 0.14-2.04), P = 0.024], BMI [β: 0.54 kg m(-2) , (0.23-0.83), P < 0.0001], and WC [β: 1.07 cm, (0.24-1.90), P = 0.011]. Moderate-equivalent PA attenuated the effect of FTO on BMI (P[interaction]  = 0.020). Among inactive individuals, FTO increased BMI by 1.06 kg m(-2) per allele (P = 0.024), whereas the increase in BMI was substantially attenuated among active individuals (0.16 kg m(-2) , P = 0.388). We observed similar effects for WC (P[interaction]  = 0.005): the FTO risk allele increased WC by 2.72 cm per allele among inactive individuals but by only 0.49 cm in active individuals. CONCLUSIONS: PA attenuates the effect of FTO genotype on BMI and WC. This may have important public health implications because genetic susceptibility to obesity in the presence of FTO variants may be reduced by adopting a physically active lifestyle.

Fat mass- and obesity-associated genotype, dietary intakes and anthropometric measures in European adults: the Food4Me study

The interplay between the fat mass- and obesity-associated (FTO) gene variants and diet has been implicated in the development of obesity. The aim of the present analysis was to investigate associations between FTO genotype, dietary intakes and anthropometrics among European adults. Participants in the Food4Me randomised controlled trial were genotyped for FTO genotype (rs9939609) and their dietary intakes, and diet quality scores (Healthy Eating Index and PREDIMED-based Mediterranean diet score) were estimated from FFQ. Relationships between FTO genotype, diet and anthropometrics (weight, waist circumference (WC) and BMI) were evaluated at baseline. European adults with the FTO risk genotype had greater WC (AA v. TT: +1·4 cm; P=0·003) and BMI (+0·9 kg/m2; P=0·001) than individuals with no risk alleles. Subjects with the lowest fried food consumption and two copies of the FTO risk variant had on average 1·4 kg/m2 greater BMI (Ptrend=0·028) and 3·1 cm greater WC (Ptrend=0·045) compared with individuals with no copies of the risk allele and with the lowest fried food consumption. However, there was no evidence of interactions between FTO genotype and dietary intakes on BMI and WC, and thus further research is required to confirm or refute these findings.

How reliable is internet-based self-reported identity, socio-demographic and obesity measures in European adults?

In e-health intervention studies, there are concerns about the reliability of internet-based, self-reported (SR) data and about the potential for identity fraud. This study introduced and tested a novel procedure for assessing the validity of internet-based, SR identity and validated anthropometric and demographic data via measurements performed face-to-face in a validation study (VS). Participants (n = 140) from seven European countries, participating in the Food4Me intervention study which aimed to test the efficacy of personalised nutrition approaches delivered via the internet, were invited to take part in the VS. Participants visited a research centre in each country within 2 weeks of providing SR data via the internet. Participants received detailed instructions on how to perform each measurement. Individual's identity was checked visually and by repeated collection and analysis of buccal cell DNA for 33 genetic variants. Validation of identity using genomic information showed perfect concordance between SR and VS. Similar results were found for demographic data (age and sex verification). We observed strong intra-class correlation coefficients between SR and VS for anthropometric data (height 0.990, weight 0.994 and BMI 0.983). However, internet-based SR weight was under-reported (Δ -0.70 kg [-3.6 to 2.1], p < 0.0001) and, therefore, BMI was lower for SR data (Δ -0.29 kg m(-2) [-1.5 to 1.0], p < 0.0001). BMI classification was correct in 93 % of cases. We demonstrate the utility of genotype information for detection of possible identity fraud in e-health studies and confirm the reliability of internet-based, SR anthropometric and demographic data collected in the Food4Me study. TRIAL REGISTRATION: NCT01530139 ( http://clinicaltrials.gov/show/NCT01530139 ).

Changes in physical activity following a genetic-based internet-delivered personalized intervention: randomized controlled trial (Food4Me)

Background: There is evidence that physical activity (PA) can attenuate the influence of the fat mass- and obesity-associated (FTO) genotype on the risk to develop obesity. However, whether providing personalized information on FTO genotype leads to changes in PA is unknown. Objective: The purpose of this study was to determine if disclosing FTO risk had an impact on change in PA following a 6-month intervention.

Methods: The single nucleotide polymorphism (SNP) rs9939609 in the FTO gene was genotyped in 1279 participants of the Food4Me study, a four-arm, Web-based randomized controlled trial (RCT) in 7 European countries on the effects of personalized advice on nutrition and PA. PA was measured objectively using a TracmorD accelerometer and was self-reported using the Baecke questionnaire at baseline and 6 months. Differences in baseline PA variables between risk (AA and AT genotypes) and nonrisk (TT genotype) carriers were tested using multiple linear regression. Impact of FTO risk disclosure on PA change at 6 months was assessed among participants with inadequate PA, by including an interaction term in the model: disclosure (yes/no) × FTO risk (yes/no).

Results: At baseline, data on PA were available for 874 and 405 participants with the risk and nonrisk FTO genotypes, respectively. There were no significant differences in objectively measured or self-reported baseline PA between risk and nonrisk carriers. A total of 807 (72.05%) of the participants out of 1120 in the personalized groups were encouraged to increase PA at baseline. Knowledge of FTO risk had no impact on PA in either risk or nonrisk carriers after the 6-month intervention. Attrition was higher in nonrisk participants for whom genotype was disclosed (P=.01) compared with their at-risk counterparts.

Conclusions: No association between baseline PA and FTO risk genotype was observed. There was no added benefit of disclosing FTO risk on changes in PA in this personalized intervention. Further RCT studies are warranted to confirm whether disclosure of nonrisk genetic test results has adverse effects on engagement in behavior change.

The role of environmental and genetic influences on fatty acid taste sensitivity

 The studies conducted in this thesis add to the growing body of literature supporting the existence of fatty acid taste. Data contributes to the novel, yet mounting research for a functional role of fat taste in food intake regulation, which may have important implications for overweight and obesity.

A syntenic cross species aneuploidy genetic screen links RCAN1 expression to β-cell mitochondrial dysfunction in Type 2 diabetes

Type 2 diabetes (T2D) is a complex metabolic disease associated with obesity, insulin resistance and hypoinsulinemia due to pancreatic β-cell dysfunction. Reduced mitochondrial function is thought to be central to β-cell dysfunction. Mitochondrial dysfunction and reduced insulin secretion are also observed in β-cells of humans with the most common human genetic disorder, Down syndrome (DS, Trisomy 21). To identify regions of chromosome 21 that may be associated with perturbed glucose homeostasis we profiled the glycaemic status of different DS mouse models. The Ts65Dn and Dp16 DS mouse lines were hyperglycemic, while Tc1 and Ts1Rhr mice were not, providing us with a region of chromosome 21 containing genes that cause hyperglycemia. We then examined whether any of these genes were upregulated in a set of ~5,000 gene expression changes we had identified in a large gene expression analysis of human T2D β-cells. This approach produced a single gene, RCAN1, as a candidate gene linking hyperglycemia and functional changes in T2D β-cells. Further investigations demonstrated that RCAN1 methylation is reduced in human T2D islets at multiple sites, correlating with increased expression. RCAN1 protein expression was also increased in db/db mouse islets and in human and mouse islets exposed to high glucose. Mice overexpressing RCAN1 had reduced in vivo glucose-stimulated insulin secretion and their β-cells displayed mitochondrial dysfunction including hyperpolarised membrane potential, reduced oxidative phosphorylation and low ATP production. This lack of β-cell ATP had functional consequences by negatively affecting both glucose-stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Thus, from amongst the myriad of gene expression changes occurring in T2D β-cells where we had little knowledge of which changes cause β-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to β-cell mitochondrial dysfunction in T2D.